Difference between revisions of "General Information/ Relationship Between IS and Eukaryotic TE"

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'''<big>I</big>'''n spite of their obvious similarities, there is often poor transfer of knowledge between studies of prokaryotic and of eukaryotic TE. This artificial barrier is reflected in their nomenclature systems: Prokaryotic TE are named following the basic logic of bacterial genetics built on the initial Demerec rules<ref><nowiki><pubmed>5961488</pubmed></nowiki></ref>; Eukaryotic TE, on the other hand, have more colorful names in keeping with the culture of nomenclature used in eukaryotic genetics. To a certain extent, this camouflages the diversity and relationships between members of the eukaryotic TE superfamilies and their prokaryotic cousins.
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'''<big>I</big>'''n spite of their obvious similarities, there is often poor transfer of knowledge between studies of prokaryotic and of eukaryotic TE. This artificial barrier is reflected in their nomenclature systems: Prokaryotic TE are named following the basic logic of bacterial genetics built on the initial [[wikipedia:Milislav_Demerec|Demerec]] rules<ref><pubmed>5961488</pubmed></ref>; Eukaryotic TE, on the other hand, have more colorful names in keeping with the culture of nomenclature used in eukaryotic genetics. To a certain extent, this camouflages the diversity and relationships between members of the eukaryotic TE superfamilies and their prokaryotic cousins.
  
It is important to appreciate that the basic chemistry of transposition is identical for both prokaryotic and eukaryotic elements<ref><nowiki><pubmed>7801124</pubmed></nowiki></ref><ref><nowiki><pubmed>20067338</pubmed></nowiki></ref><ref><nowiki><pubmed>26104718</pubmed></nowiki></ref><ref><nowiki><pubmed>8696976</pubmed></nowiki></ref><ref><nowiki><pubmed>21439812</pubmed></nowiki></ref><ref><nowiki><pubmed>11774877</pubmed></nowiki></ref>. Moreover, many eukaryotic DNA transposons have similar sizes and organization to those of prokaryotic IS and, since most do not carry additional “passenger” genes, they are not transposons in the prokaryotic sense and should strictly be considered as eukaryotic IS. The major differences lie in how Tpase expression and activity is regulated<ref><nowiki><pubmed>15207871</pubmed></nowiki></ref>. One important difference is that most eukaryotic transposons are “insulated” by constraints of the nucleus (which physically separate the transposition process from that of Tpase expression) while those of prokaryotes are not since prokaryotic transcription and translation are coupled. In addition, eukaryotic transposons are subject to a hierarchy of regulation via small RNAs<ref><nowiki><pubmed>23145453</pubmed></nowiki></ref><ref><nowiki><pubmed>24280023</pubmed></nowiki></ref><ref><nowiki><pubmed>30304932</pubmed></nowiki></ref><ref><nowiki><pubmed>21074719</pubmed></nowiki></ref>. In prokaryotes, it is possible that [https://pt.wikipedia.org/wiki/CRISPR CRISPRs] may impose some control at this level but, although it has been demonstrated that CRISPRs are active against mobile genetic elements and may regulate some endogenous gene expression [see <ref><nowiki><pubmed>24273648</pubmed></nowiki></ref>], these are limited to plasmids and phage and to our knowledge have not yet been demonstrated to act on intracellular MGE such as IS and transposons.  
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It is important to appreciate that the basic chemistry of transposition is identical for both prokaryotic and eukaryotic elements<ref><pubmed>7801124</pubmed></ref><ref><pubmed>20067338</pubmed></ref><ref><pubmed>26104718</pubmed></ref><ref><pubmed>8696976</pubmed></ref><ref><pubmed>21439812</pubmed></ref><ref><pubmed>11774877</pubmed></ref>. Moreover, many eukaryotic DNA transposons have similar sizes and organization to those of prokaryotic IS and, since most do not carry additional “passenger” genes, they are not transposons in the prokaryotic sense and should strictly be considered as eukaryotic IS. The major differences lie in how Tpase expression and activity is regulated<ref><pubmed>15207871</pubmed></ref>. One important difference is that most eukaryotic transposons are “insulated” by constraints of the nucleus (which physically separate the transposition process from that of Tpase expression) while those of prokaryotes are not since prokaryotic transcription and translation are coupled. In addition, eukaryotic transposons are subject to a hierarchy of regulation via small RNAs<ref><pubmed>23145453</pubmed></ref><ref><pubmed>24280023</pubmed></ref><ref><pubmed>30304932</pubmed></ref><ref><pubmed>21074719</pubmed></ref>. In prokaryotes, it is possible that [https://pt.wikipedia.org/wiki/CRISPR CRISPRs] may impose some control at this level but, although it has been demonstrated that [[wikipedia:CRISPR|CRISPRs]] are active against mobile genetic elements and may regulate some endogenous gene expression [see <ref><pubmed>24273648</pubmed></ref>], these are limited to plasmids and phage and to our knowledge have not yet been demonstrated to act on intracellular Mobile Genetic Element such as IS and transposons.  
  
In spite of these differences, a significant number of eukaryotic DNA TE are related to prokaryotic IS ([[General Information/What Is an IS?#Characteristics of insertion sequence families|Table Characteristics of IS families]]; [[General Information/Major Groups are Defined by the Type of Transposase They Use#Transposases examined by secondary structure prediction programs|Table MGE transposases examined by secondary structure prediction programs]]), and moreover, eukaryotic TE including passenger genes are now being identified [see e.g. <ref><nowiki><pubmed>23548000</pubmed></nowiki></ref>]. This reinforces the view that the borders between different types of TE are “fuzzier” than previously recognized.
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In spite of these differences, a significant number of eukaryotic DNA TE are related to prokaryotic IS ([[General Information/What Is an IS?#Characteristics of insertion sequence families|Table Characteristics of IS families]]; [[General Information/Major Groups are Defined by the Type of Transposase They Use#Transposases examined by secondary structure prediction programs|Table MGE transposases examined by secondary structure prediction programs]]), and moreover, eukaryotic TE including passenger genes are now being identified [see e.g. <ref><pubmed>23548000</pubmed></ref>]. This reinforces the view that the borders between different types of TE are “fuzzier” than previously recognized.
  
 
==Bibliography==
 
==Bibliography==
 
<references />
 
<references />

Latest revision as of 21:07, 9 August 2021

In spite of their obvious similarities, there is often poor transfer of knowledge between studies of prokaryotic and of eukaryotic TE. This artificial barrier is reflected in their nomenclature systems: Prokaryotic TE are named following the basic logic of bacterial genetics built on the initial Demerec rules[1]; Eukaryotic TE, on the other hand, have more colorful names in keeping with the culture of nomenclature used in eukaryotic genetics. To a certain extent, this camouflages the diversity and relationships between members of the eukaryotic TE superfamilies and their prokaryotic cousins.

It is important to appreciate that the basic chemistry of transposition is identical for both prokaryotic and eukaryotic elements[2][3][4][5][6][7]. Moreover, many eukaryotic DNA transposons have similar sizes and organization to those of prokaryotic IS and, since most do not carry additional “passenger” genes, they are not transposons in the prokaryotic sense and should strictly be considered as eukaryotic IS. The major differences lie in how Tpase expression and activity is regulated[8]. One important difference is that most eukaryotic transposons are “insulated” by constraints of the nucleus (which physically separate the transposition process from that of Tpase expression) while those of prokaryotes are not since prokaryotic transcription and translation are coupled. In addition, eukaryotic transposons are subject to a hierarchy of regulation via small RNAs[9][10][11][12]. In prokaryotes, it is possible that CRISPRs may impose some control at this level but, although it has been demonstrated that CRISPRs are active against mobile genetic elements and may regulate some endogenous gene expression [see [13]], these are limited to plasmids and phage and to our knowledge have not yet been demonstrated to act on intracellular Mobile Genetic Element such as IS and transposons.

In spite of these differences, a significant number of eukaryotic DNA TE are related to prokaryotic IS (Table Characteristics of IS families; Table MGE transposases examined by secondary structure prediction programs), and moreover, eukaryotic TE including passenger genes are now being identified [see e.g. [14]]. This reinforces the view that the borders between different types of TE are “fuzzier” than previously recognized.

Bibliography

  1. Demerec M, Adelberg EA, Clark AJ, Hartman PE . A proposal for a uniform nomenclature in bacterial genetics. - Genetics: 1966 Jul, 54(1);61-76 [PubMed:5961488]
  2. Dyda F, Hickman AB, Jenkins TM, Engelman A, Craigie R, Davies DR . Crystal structure of the catalytic domain of HIV-1 integrase: similarity to other polynucleotidyl transferases. - Science: 1994 Dec 23, 266(5193);1981-6 [PubMed:7801124] [DOI]
  3. Hickman AB, Chandler M, Dyda F . Integrating prokaryotes and eukaryotes: DNA transposases in light of structure. - Crit Rev Biochem Mol Biol: 2010 Feb, 45(1);50-69 [PubMed:20067338] [DOI]
  4. Hickman AB, Dyda F . Mechanisms of DNA Transposition. - Microbiol Spectr: 2015 Apr, 3(2);MDNA3-0034-2014 [PubMed:26104718] [DOI]
  5. Rice P, Craigie R, Davies DR . Retroviral integrases and their cousins. - Curr Opin Struct Biol: 1996 Feb, 6(1);76-83 [PubMed:8696976] [DOI]
  6. Montaño SP, Rice PA . Moving DNA around: DNA transposition and retroviral integration. - Curr Opin Struct Biol: 2011 Jun, 21(3);370-8 [PubMed:21439812] [DOI]
  7. Rice PA, Baker TA . Comparative architecture of transposase and integrase complexes. - Nat Struct Biol: 2001 May, 8(5);302-7 [PubMed:11774877] [DOI]
  8. Nagy Z, Chandler M . Regulation of transposition in bacteria. - Res Microbiol: 2004 Jun, 155(5);387-98 [PubMed:15207871] [DOI]
  9. Fedoroff NV . Presidential address. Transposable elements, epigenetics, and genome evolution. - Science: 2012 Nov 9, 338(6108);758-67 [PubMed:23145453] [DOI]
  10. Dumesic PA, Madhani HD . Recognizing the enemy within: licensing RNA-guided genome defense. - Trends Biochem Sci: 2014 Jan, 39(1);25-34 [PubMed:24280023] [DOI]
  11. Russell SJ, LaMarre J . Transposons and the PIWI pathway: genome defense in gametes and embryos - Reproduction: 2018 Oct 1, 156(4);R111–R124 [PubMed:30304932] [DOI]
  12. Saito K, Siomi MC . Small RNA-mediated quiescence of transposable elements in animals. - Dev Cell: 2010 Nov 16, 19(5);687-97 [PubMed:21074719] [DOI]
  13. Bikard D, Marraffini LA . Control of gene expression by CRISPR-Cas systems. - F1000Prime Rep: 2013, 5;47 [PubMed:24273648] [DOI]
  14. Bao W, Jurka J . Homologues of bacterial TnpB_IS605 are widespread in diverse eukaryotic transposable elements. - Mob DNA: 2013 Apr 1, 4(1);12 [PubMed:23548000] [DOI]